Zheng Yifeng, Martin-Morales Agustin, Wang Jing, Fujishima Masaki, Okumura Eri, Sato Kenji
Division of Applied Biosciences, Graduate School of Agriculture, Kyoto University, Kitashirakawa Oiwake-cho, Kyoto, Japan.
Research & Development Group, Sun Chlorella Co., Ltd., Osaka-cho, Kyoto, Japan.
NPJ Sci Food. 2021 Jul 23;5(1):22. doi: 10.1038/s41538-021-00105-3.
This study examined the effects of oral administration of water extract of chlorella (WEC) (100 mg/kg bodyweight) and phenethylamine (10 μg/kg bodyweight) on high-fat diet (HFD)-induced liver damage in mice. Phenethylamine significantly mitigated HFD-induced lipid oxidation (generation of malondialdehyde) and liver damage without markedly decreasing hepatic lipid accumulation. WEC exerted similar effects although with decreased efficacy. In addition, WEC and phenethylamine decreased the methylglyoxal levels and increased the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels in the liver. Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These facts indicate that methylglyoxal triggers oxidation of accumulated lipid, which generates malondialdehyde and consequently induces liver damage. Suppression of generation of toxic aldehydes by WEC and phenethylamine was also confirmed by maintaining hepatic cysteine, highly reactive to aldehydes. Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH.
本研究考察了口服小球藻水提取物(WEC,100毫克/千克体重)和苯乙胺(10微克/千克体重)对高脂饮食(HFD)诱导的小鼠肝损伤的影响。苯乙胺显著减轻了HFD诱导的脂质氧化(丙二醛生成)和肝损伤,而未明显降低肝脏脂质蓄积。WEC也发挥了类似作用,不过效果较弱。此外,WEC和苯乙胺降低了肝脏中甲基乙二醛水平,并提高了甘油醛-3-磷酸脱氢酶(GAPDH)蛋白水平。甲基乙二醛由GAPDH的底物磷酸二羟丙酮和3-磷酸甘油醛生成。这些事实表明,甲基乙二醛引发蓄积脂质的氧化,生成丙二醛,进而诱导肝损伤。通过维持对醛高度反应的肝半胱氨酸,也证实了WEC和苯乙胺对有毒醛类生成的抑制作用。因此,痕量苯乙胺通过增加GAPDH来调节甲基乙二醛,从而减轻HFD诱导的肝损伤。